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Bone turnover is a continuous process that ensures calcium homeostasis and bone quality [ 75].
Baseline bone turnover is a major determinant of bisphosphonates skeletal uptake (Lin, 1996).
Subchondral bone turnover is a well-defined component of OA [ 4].
Also, neonatal bone turnover is a potential endogenous source of lead in infant blood (Gulson et al. 2001).
Cartilage and bone turnover is a complex process in which proteinases play a prominent role in health and disease.
These results confirmed that imaging of cathepsin activity, MMP activity, and bone turnover is a successful non-invasive diagnostic modality, capable of providing robust measures of disease progression.
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Although leptin may play some role in the effects of high fat feeding in vivo [16], its main action on bone turnover is an indirect stimulation of bone resorption via effects on RANKL expression [16].
These results are not entirely surprising because bone turnover is an intricate balance of formation and osteolysis mediated in tight cooperation by osteoclasts and osteoblasts [10]– [10].
Changes in the rate of bone turnover are an important determinant of bone disease because alterations in bone turnover rate have been associated with an increased fracture risk.
Measurement of biochemical markers of bone turnover is therefore becoming a more widely used end-point in clinical trials in postmenopausal osteoporosis.
The deterioration of trabecular microarchitecture induced by elevated bone turnover is increasingly recognized as a factor in the pathogenesis of osteoporotic fractures.
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